ReviewBiomedicines2025
Advanced Research in the Pathophysiology of Venous Thromboembolism-Acute Pulmonary Embolism.
Review in Biomedicines, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed.
- Admission Endothelial Activation and Stress Index and Echocardiographic RV-PA Coupling for Early Risk Stratification in Intermediate-Risk Acute Pulmonary Embolism.Journal of clinical medicine · 2026Article
- Risk Stratification in Pulmonary Embolism: Prognostic Value of PESI, WELLS, PADUA, and IMPROVE Scores in Relation to Laboratory Markers.Journal of clinical medicine · 2026Article
- Article
- The Interplay Between Obesity and Venous Thromboembolism: From Molecular Aspects to Clinical Issue.International journal of molecular sciences · 2025Review
- The Role of Early Rehabilitation in Treatment of Acute Pulmonary Embolism-A Narrative Review.Journal of clinical medicine · 2025Review
- Article
- Association between the platelet-to-albumin ratio and 28-day all-cause mortality in critically ill patients with Pulmonary embolism: a retrospective cohort study and predictive model establishment based on machine learning.Frontiers in medicine · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
According to the literature, cardiovascular diseases (CVDs)-including myocardial infarction, stroke, and venous thromboembolism (VTE)-are among the leading causes of mortality and morbidity worldwide. Evidence suggests that CVDs share common risk factors and pathophysiological mechanisms. Similar to the Mosaic Theory of Hypertension proposed by Irvine Page in 1949, the pathophysiology of VTE is multifactorial, involving multiple interacting processes. The concept of immunothrombosis, introduced by Engelmann and Massberg in 2009, describes the interplay between the immune system and thrombosis. Both thrombosis and hemostasis share core mechanisms, including platelet activation and fibrin formation. Additionally, immune mediators-such as monocytes, neutrophil extracellular traps (NETs), lymphocytes, selectins, and various molecular factors-play a critical role in thrombus formation. This review highlights inflammation as a key risk factor for pulmonary embolism (APE). Immunity is central to the complex interactions among the coagulation cascade, platelets, endothelium, reactive oxygen species (ROS), and genetic factors. Specifically, we examine the roles of the endothelium, immune cells, and microRNAs (miRNAs) in the pathophysiology of APE and explore potential therapeutic targets. This review aims to elucidate the roles of the endothelium, immune cells, and miRNAs in the pathophysiology of APE and explore potential future perspective.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.